The naturally occurring C-nucleoside formycin has demonstrated a broad range of biological properties (e.g., antitumor) which have emanated from its isomeric relationship with adenosine. To date, the complete chemotherapeutic potential of formycin has been limited by its rapid deactivation in vivo by adenosine deaminase. A number of studies have arisen to account for this propensity for adenosine deaminase. This led to a recent hypothesis which says that the pi-bonding arrangement in and stereochemical environment around the heterocyclic base unit of formycin are controlling factors in the adenosine deaminase affinity for this nucleoside. Therefore, in order to verify this conclusion, several analogs of formycin (namely 7-amino-3-(beta-D-ribofuranosyl)isoxazolo(4,5-d)pyrimidine, 7-amino-3-(beta-D-ribofuranosyl)isoxazolo (4,3-d)pyrimidine, 8-amino-1-methyl-3-(beta-D-ribofuranosyl)-1H-pyrazolo (3,4-g)quinazoline, and 4-amino-7-(beta-D-ribofuranosyl)pyrazolo(3,4-e) (1,3)oxazine), whose heterocyclic bases possess specific pi-bonding patterns without attendant steric probes, will be prepared and biologically evaluated against adenosine deaminase.